Erythema multiforme


Hypersensitivity reaction that usually follows infections such as herpes simplex virus or mycoplasma.

Major cause felt to be herpes virus.

Infections are common causes in children.

Herpes simplex most common cause in young adults.

Mycoplasma pneumoniae most prevalent bacterial agent associated.

Thought to be the result of an immune mediated hypersensitivity reaction that is most commonly mediated by HSV-1 and 2, mycoplasma pneumoniae or drugs.

Drugs such as nonsteroidal anti-inflammatory drugs, antibiotics, antiepileptics, malignant processes, menstruation, and inflammatory bowel disease are all associated.

Approximately 50% of cases idiopathic without a precipitating factor.

Sudden onset of raised, symmetric targetoid macules and thin plaques on the arms, legs, hands and feet.

Characterized by eruption of macules, papules, and target lesions that are often symmetrical on the extremities.

Target lesions help distinguish the process from Stevens Johnson syndrome, a similar skin condition that presents with confluent purpuric macules and severe mucosal erosions. Mucosal involvement is usually minimal.

Most frequent lesions on the dorsal hands and feet, extensor limbs, elbows, and knees.

Rarely associated with bullae, sloughing and mucosal involvement.

Involvement may include the oral mucosa, labial mucosal, ocular mucosa and less frequently the upper respiratory and pharyngeal mucosa.

Desquamation of the skin is present, usually does not exceed 10%.

Histological findings include lymphocytic infiltrate at dermal-epidermal junction and around blood vessels, with dermal edema necrosis of epidermal keratinocytes, and bullae formation.

Histologically peri vascular dermal lymphohistiocytic infiltrates with some eosinophils, edema in the epidermis and vacuolar degeneration of basal cells.

Classic lesion is a target with three zones-a central purpura , and elevated edematous ring, and a surrounding macula erythema.

High density of T lymphocytes in infiltrate.

Appears to be the result of TH1-mediated immune response to an inciting events such as drug exposure, infections such as HSV, HCV, and mycoplasma pneumoniae.

Incidence estimated to be 0.01-1%.

Male: female ratio 3:2-2:1.

All ages affected with peak incidence 2-4th decades and 20% of cases in children an adolescents.

Rare below age 3 and over the age of 50 years.

Occurs more commonly in younger patients while toxic epidermal necrolysis and Stevens-Johnson syndrome occur more commonly in older individuals.

Usually sudden onset of symmetrical cutaneous and/or mucocutaneous lesions with concentric color changes in some or all lesions.

Pruritus is usually not present but burning sensation is.

Flu-like prodrome seen in at least 50% of patients 1-14 days before skin lesions appear.

Most cases resolve without problems within 2-4 weeks.

Usually resolves without complications.

Not associated with mortality.

Hallmark lesions are targeted lesions typically acral with symmetric extensor surface involvement.

Lesions are symmetrically distributed, erythematous macules or papules and evolving into iris or target lesions, with red borders and petechiae and vesicle purpuric changes.

Classically targetoid lesions that are round and papular with central duskiness will blister formation, with the clear ring of edema surrounded by an erythematous halo.

Classically the lesions have the appearance of a target with three zones of color change.

Coalescence of lesions may occur and become a generalized rash.

Vesiculobullous lesions may develop.

Palms, soles, dorsum of hands, extensor extremity involvement and facial lesions predominate.

May lead to hyperpigmentation or hypopigmentation following recovery.

10% have associated eye involvement with purulent conjunctivitis and increased tearing.

25% experience mucous membrane blisters involving the oral cavity.

Acute erythema multiforme lesions appear within a few days and resolved within 2-6 weeks.

Some cases of EM are not self-limited and can recur.

Rarely lesions do not resolve and are persistent EM lesions, despite therapy.

History and physical examination are often sufficient for diagnosis, however a biopsy may be needed to rule out other processes.

Mild cases require only symptomatic treatment with analgesics or NSAIDs, compresses with saline or Burow’s solution or topical steroids, and oral histamines.

In its mildest forms, it is a self-limited process, with each episode lasting 1 to 4 weeks.

The bullous form includes a spectrum of Stevens-Johnson syndrome and toxic epidermal necrolysis.

For severe mucocutaneous involvement oral corticosteroids may be necessary.

Drugs associated with EM must be discontinued and any associated infection should be treated.

In patients with recurrent EM related to HSV continuous antiviral therapy is recommended for six months to prevent recurrence.

In recurrent disease immunomodulatory agents include azathioprine, mycophenolate, dapsone, and thalidomide can be tried in patients not responsive to antiviral therapy.

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